Endocrine Immunology of Chagas Disease.

Abstract

The concept of immunoendocrine interactions, existing in normal and pathological conditions, is relatively recent. Accordingly, cells from the immune system and from endocrine glands share common receptors for cytokines and hormones, allowing systemic and local regulatory mechanisms. In this context, lymphoid organs are under physiological hormonal control. Disturbances in these systems, as those caused by pathogens changes the physiological profile of these interactions, with the release of proinflammatory cytokines and hormones, and one example is the hypothalamus-pituitary-adrenal (HPA) axis. Within endocrine tissues, inflammation occurs with local increase of cytokines, extracellular matrix proteins, and influx of inflammatory cells. One example of lymphoid organ that can be influenced by pathogens and hormonal response is the thymus, with changes in the normal T-cell differentiation process. Several viruses, bacteria, and protozoa induce severe thymic atrophy with massive death of developing thymocytes. In several conditions, this is at least partially due to the activation of the HPA axis and ultimate rise in systemic glucocorticoid release. In the case of Trypanosoma cruzi infection (a protozoan that is the causative agent of Chagas disease), another stress-related hormone, prolactin can partially revert this pathogen-induced thymic atrophy and the abnormal release of immature thymocytes from the organ. Overall, our data clearly reveal that pathogens and more particularly T. cruzi, can promote an immunoendocrine imbalance, with emphasis on stress-related hormones, which can influence lymphocyte dynamics, with consequences in the system and local immune response.